23. Duodenal Ulcer

Peptic duodenal ulcer

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History (1)

Diocles of Carystos (350 b.c.) - melancholic gassy illness originating in the stomach – (Yamada et al.)

Marcello Donati – first gastric ulcer (1586) 1975 – China - 60 year old man with prepiloric

perforated ulcer (167 b.c.) 1688 - Muralto – first ulcer description 1727 – C. Rawlison – first gastric perforation

1746 – G. Hamberger - first duodenal perforation

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History (2)

1881 – Rydigier – first gastric resection for ulcer

1884 – Mikulicz first attempt of suturing a peptic ulcer perforation

1912 – Bircher – vagotomy in ulcer surgery

1943 - L. Dragsted and H. Owens – troncular vagotomy

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Definition

A breach, mostly circumscribed of the gastric or duodenal wall beyond muscularis mucosae.

Erosion – a breach limited only to the mucosa

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Classification

Gastric

Duodenal:

Bulbar

Postbulbar

Anastomotic Stress ulcer (Curling or Cushing ulcers, in

sepsis) Endocrine ulcer (Zollinger-Ellison)

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Classification

Histology Acute Chronic

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Classification of benign gastric ulcers (after Johnson, 1957)

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Acute superficial:

Single or multiple ('erosions')

Chronic:

Type I, usually lesser curve

Type II, combined with duodenal ulcer

Type III, prepyloric

Type IV, proximal stomach <2 cm from oesophageal junction

Epidemiology 1

5-10% in western world (300.000 new cases in USA)

The 1-year point prevalence of active gastric and duodenal ulcer in the United States is approximately 1.8%

In 1998, it was estimated that there were 6.8 million cases of PUD in the United States, representing a prevalence rate of 2490 cases per 100,000 persons.

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Epidemiology 2

Duodenal/gastric ulcer ratio is variableMale:Female ratio=2-1 (clasically 4(6)-1)More than 75% of patients with PUD are

of working age (18 to 65 years)

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Stomach, gross and histology

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From http://www.training.seer.cancer.gov

Anatomy

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Vascularization

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Nyhus et al.

Vagus nerve into the abdomen - Testut

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Inervation

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Nyhus et al.

Lymphatics

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Nyhus et al.

Gastric secretion

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Gastric secretion regulation

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Gastric secretion regulation

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Nyhus et al.

Pathogenesis (1)

Gastric secretion changes in peptic ulcer patients Increased BAO (normal: 0-10 mmol/hr)

Nocturnal increase of gastric output

Increased PCM

Exagerated response to stimuli (hystamine), hypoglicemia, mechanical stimuli

Hypervagotony

Anomalous gastric secretion inhibition (secretin)

Ohne magensaft kein peptisches geschwür – K. Schwartz, 1911

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Pathogenesis (2)

Gastric secretion regulation changes:

High output of gastrin as a response to different stimuli

Anomalous negative feed-back of gastric secretion gastrin-mediated

Somatostatin secretion inhibition

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Pathogenesis (3)

Duodenal mucosa changes in peptic ulcer patients:

Prostaglandins deficit

Bicarbonate deficit

Diminished duodenal mucus

Helicobacter pylori (metaplasia)

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Pathogenesis (4)

Genetics

Environment NSAID

Smoking

Stress

Drugs (cocaine, crack)

Helicobacter pylori

Alimentary (alcohol etc.)

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Helicobacter pylori

1975 - Howard Steer 1989 - J. R. Warren, B. J. Marshall In 40-60% of western population 100% in tropics and the third world More frequent in urban aria

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Helicobacter pylori

Coco-bacil Gram negative with multiple enzymes

50% are producing Vac A

cag A – higher virulence

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Helicobacter pylori - genome

S SUERBAUM, M.D.,P MICHETTI, M.D. - N Engl J Med, Vol. 347, No. 15,2002

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Click to edit Master text stylesSecond level

Third levelFourth level

Fifth level

H. pylori interaction

S SUERBAUM, M.D.,P MICHETTI, M.D. - N Engl J Med, Vol. 347, No. 15,2002

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Cliodna A M McNulty, Judith I Wyatt - Helicobacter pylori – J Clin Pathol 1999;52:338-344

Helicobacter pylori

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Helicobacter pylori

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Helicobacter pylori

Produces hypergastrinemia and hyperacidity (hypotheses):

Inhibitory protein synthesis acting on gastrin releasing cells

Direct inhibition of somatostatin

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Helicobacter pylori

Direct disruption of mucosa and influencing cytokines or of the phospholipase

Activating the macrophages, TNF (Tumor Necrosis Factor), IL1 synthesis, and oxygen free radicals;

Autoantibodies production

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Ulcer equation

ulcer

Clorhidro-peptic secretion

Mucus

Epithelium

Bicarbonate secretion

Vascularization

Genetic factors

Stres s

Smoking

MEN

NSAID

H. pylori

Smoking

Cirrhos is

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Fifth level

H. pylori infection – natural history - S SUERBAUM, M.D.,P MICHETTI, M.D. - N Engl J Med, Vol. 347,No. 15,2002

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Morfopatholoy

Microscopy (Askanazy) – 4 strata

Exudative - detritus, fibrin, germs or even yeasts

Necrosis – (fibrinoid) with inflammatory infiltrate (active region)

Granulation strata

Fibrosis

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Pathology (1)

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Pathology (2)

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Clinical signs

Pain

Periodicity (with meals and seasonal)

Aching pain

Vomiting

Habitus

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Essentials of diagnosis

Epigastric pain relieved by food or antacids.

Epigastric tenderness.

Normal or increased gastric acid secretion.

Signs of ulcer disease on upper gastrointestinal x-rays or endoscopy.

Evidence of Helicobacter pylori infection.

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Lab&explorations

Laboratory

Gastrin in serum (normal < 100 pg/mL) – over 200 pg/mL in Zollinger-Ellison syndrome

Secretory tests (no longer in use)

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Lab&explorations

Endoscopy is the principal method of diagnosis, as it enables biopsies to be taken to exclude malignancy in gastric ulcers, and to do a rapid urease test or histological examination for Helicobacter.

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Endoscopy

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On open-access endoscopy for 'dyspepsia', about 12% per cent of patients have duodenal ulcer and 3% gastric ulcer, but the numbers and ratios vary with age. Every gastric ulcer should be suspected of being malignant until proved benign by multiple biopsies and complete endoscopic healing.

Radiology

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Radiographic studies

Deformities and an ulcer niche.

Inflammatory swelling and scarring may lead to distortion of the duodenal bulb, eccentricity of the pyloric channel, or pseudodiverticulum formation.

The ulcer itself may be seen either in profile or, more commonly, en face.

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Helicobacter pylori testing

Noninvasive

14C breath test

Serology

Stool antigen determination

Endoscopy

Direct examination and test

Cultures


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Detection and Treatment of Helicobacter pylori Infection in Adult Patients

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Peptic ulcer evolution

Recurrence

Complications

Hemorrhage

Perforation

Penetration

Stenosis

Malignancy (only for gastric ulcers)

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Zollinger-Elison syndrome

Zollinger and Ellison defined the syndrome that now bears their names – 1955

Triad of

severe ulcer disease,

gastric acid hypersecretion, and

non-beta islet cell tumors of the pancreas

0.1 to 1% of patients with peptic ulcer disease

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Gastrinomas: Origin and Classification

One third (15% to 77% in different studies) of patients with gastrinomas have multiple endocrine neoplasia type 1 (MEN-1)

MEN-1 is an autosomal dominant genetic disorder associated with a high degree of penetrance

Patients with MEN-1 may have involvement of all three organs (parathyroids, pancreatic islets, and pituitary)

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Zollinger-Elison syndrome

The tumor may be single or multiple and can range in size for less than 1 cm to more than 3 cm.

When associated with MEN-1, studies suggest that gastrinomas are usually multiple and commonly found within the duodenum and pancreas

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Diagnostic

Difficult to find

Serum gastrin – over 200 pg/ml

Secretin provocative test

US

CT-scan

EUS

Angiography with sampling

MRI

Portal venous sampling for serum levels of gastrin

IOUS

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Treatment

Medical

PPI – large doses

BAO measuring

Surgical

Tumor excision, or

Total gastrectomy, and

Metastazis treatment

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Upper digestive hemorrhage

Definition

Hematemesis – vomiting blood

Melena – the passage of black, tarry stools composed largely of blood that has been acted on by gastric juices, indicative of bleeding in the upper digestive tract.

Hemochezia – red blood in stools

Rebleeding - hematemesis and/or melena with shock (pulse>100b/min, CVP drop of 5 mm Hg or drop in HGB level with 2g. Confirmation needs endoscopic reevaluation

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Upper digestive hemorrhage

Diagnostic %

Ulcer 35-50

Erosions (ulcerations) 8-15

Esophagitis 5-15

Varices (gastro-esophageal)

5-15

Mallory-Weiss syndrome 15

Malignancy 1

Vascular malformation 5

Rare 5

After British Society of Gastroenterology – Gut 2002;51(suppl. IV):iv1-iv665

Bleeding risk (endoscopic assessment)

Sign % of rebleed

Arterial bleeding 90

Visible vessel 50

Fresh clot in ulcer crater 25

Small bleeding without vessel <20

Dark spot, red spot <10Freeman ML – The current endoscopic diagnosis and intensive care unit management of severe ulcer and non-variceal upper gastrointestinal hemorrhage – Gastrintest Endosc Clin North Am 1991, 1:229 66

Hemorrhagic ulcer

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Forrest tip IIbFeldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.

Hemorrhagic ulcer

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Ulcer perforation (1)

Brutal debut

Severe generalized abdominal pain

Shock

Loss of bowel sounds

Board-like rigidity of the abdominal wall

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Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.


Diagnostic (Mondor triad)

Pain (specific characteristics)

History for ulcer or dispepsia

Guarding or, more frequently abdominal wall rigidity

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Radiology (pneumoperitoneum) – in 50-75% of cases

Administration of oral soluble radiographic contrast may demonstrate a leak.

Barium studies should be avoided when perforation is suspected.

Endoscopy should not be performed.

In rare cases, urgent laparotomy is required to make the diagnosis.

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Pneumoperitoneum

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Ecografie evidenţiind pneumoperitoneu

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Stenosis (gastric outlet syndrome)

Gastric outlet obstruction is the least common complication of peptic (pyloric channel or duodenal) ulcer disease (classically 1-3%).

Two stages:

Functional (edema and inflammation surrounding an acute ulcer, especially in the antrum or pyloric channel)

Organic (scarring with fibrosis and outlet narrowing)

▪ Sistolic phase

▪ Asistolic phase

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Gastric outlet syndrome

Postprandial epigastric fullness, early satiety, and vomiting of materials ingested hours to days previously.

Vomiting may be worse toward the end of the day.

If gastric outlet obstruction is chronic, patients may develop hypochloremic alkalosis, tetany, weight loss, and, rarely, aspiration pneumonia.

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Gastric outlet syndrome

A succussion splash may be audible on physical examination.

The diagnosis may be confirmed using radiographic (barium), endoscopic, or scintigraphic (gastric-emptying) studies

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Gastric outlet syndrome - treatment

Nasogastric tube to fully evacuate the stomach

Intravenous replacement of fluid and electrolytes is imperative

Intensive antisecretory therapy with intravenous H2RAs or proton-pump inhibitors should be given to reduce nasogastric fluid losses and to promote ulcer healing

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Gastric outlet syndrome - treatment

Patients with chronic obstruction and signs of malnutrition should be given parenteral nutrition.

Upper GI study using water-soluble contrast - after 72 hours of gastric decompression.

About one-half to two-thirds of patients fail to improve after 5-7 days of gastric aspiration.

Up to 90% of cases of gastric outlet obstruction will come to either surgical or endoscopic dilatation within 1 year.

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Treatment

Drugs Antiacids

Cytoprotective agents - Sucralfate is a complex sucrose salt in which the hydroxyl groups have been substituted by aluminum hydroxide and sulfate. This compound is insoluble in water and becomes a viscous paste within the stomach and duodenum, binding primarily to sites of active ulceration.

Adverse effects - chronic renal insufficiency to prevent aluminum-induced neurotoxicity. Hypophosphatemia and gastric bezoar formation have also been rarely reported. (1 g four times per day)

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Anticholinergics

Designed to inhibit activation of the muscarinic receptor in parietal cells, met with limited success due to their relatively weak acid-inhibiting effect and significant side effects (dry eyes, dry mouth, urinary retention).

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Bismuth-containing compounds

Colloidal bismuth subcitrate (CBS) and bismuth subsalicylate (BSS, Pepto-Bismol)

Long-term usage with high doses, especially with the avidly absorbed CBS, may lead to neurotoxicity. These compounds are commonly used as one of the agents in an anti-H. pylori regimen

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Prostaglandin analogues

Prostaglandin analogues enhance mucous bicarbonate secretion, stimulate mucosal blood flow, and decrease mucosal cell turnover.

Misoprostol is contraindicated in women who may be pregnant, and women of childbearing age must be made clearly aware of this potential drug toxicity. (200 ug four times per day)

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H2 receptor antagonist

Four of these agents are presently available (cimetidine, ranitidine, famotidine, and nizatidine), and their structures share homology with histamine.

Presently, this class of drug is often used for treatment of active ulcers (4 to 6 weeks) in combination with antibiotics directed at eradicating H. pylori

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Proton pomp inhibitors

Omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole are substituted benzimidazole derivatives that covalently bind and irreversibly inhibit H+,K+-ATPase.

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Treatment

Goal - relief of symptoms (pain or dyspepsia), promote ulcer healing, and ultimately prevent ulcer recurrence and complications.

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PPI, proton pumpinhibitor; RBC, ranitidine bismuth citrate;R, metronidazole 400 mg, used adequatelyin many countries - P. MALFERTHEINER et al. – consensus Maastricht 2 şi 3 – 2000 şi 2005

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Hemorrhagic ulcer therapy

Vasopressors

Endoscopy

Surgery

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Fifth level

Surgery

Absolute indications Major hemorrhage

Perforation

Stenosis

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Treatment

Relative indications Repeated hemorrhage

Penetration

Arterial hypertension in hemorrhagic ulcer patients

Portal hypertension

Postbulbar ulcer

Multiple ulcers

Zollinger-Ellison syndrome

Professional risk patients

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Surgery - goals

Excision of the lesion

Lowering pH (obtain an hypoacid stomach)

Redo the continuity of the digestive tract

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Vagus nerves anatomy and vagotomy typesVP – posterior vagus, VA –anterior vagus, R. H-B –hepato-biliary r., R. C. –celiac r., N.A.M.C. – Lesser curvature anterior nerve (Latarjet), N.P.M.C. – great curvature anterior nerve, VT – troncular vagotomy, VS –selective vagotomy, VSS –parietal cell vagotomy (limit - 5-7 cm)

Vagotomia- variante

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Posterior troncular vagotomy with anterior seromiotomy (Taylor)

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Pyloroplasty

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Nyhus et al.

Suturing a perforated duodenal ulcer

Nyhus et al.

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Hemostasis in situ

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Nyhus et al.

Gastric resection (R), hemigastrectomy (H) and antrectomy (A); a. Gastroduodenoanstomy (Péan-

Billroth I), b. Gastrojejunostomy - Billroth II

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Billroth II operation and some of its modifications. (From Soybel DI, Zinner MJ: Stomach and duodenum: Operative procedures. In Zinner MJ, Schwartz SI, Ellis H [eds]: Maingot's Abdominal Operations, vol I, 10th ed. Stamford, CT, Appleton & Lange, 1997.)

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JA Myers, JW Millikan, TJ Saclarides - Common Surgical Diseases, Springer 2008

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23. Duodenal Ulcer